Severe necrosis of oesophageal and gastric mucosa in fatal methanol poisoning

Cascallana, José Luis; Gordo, Verónica; Montes, Rosario

doi:10.1016/j.forsciint.2012.01.033

Cited by 12 publications

(8 citation statements)

References 22 publications

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“…In one study from Israel over a fifteen‐year period, ingestions involved alkalis in 42% of cases, acids in 32% and household bleach in 26% . The mechanism of injury differs slightly depending on the agent involved, with acids causing coagulative necrosis, protein precipitation and eschar formation, and alkaline agents causing saponification with liquefactive necrosis enabling deeper penetration, sometimes with involvement of the muscularis propria (as in Case 1) . Although it has been stated that these features are not thought to make a significant difference to the clinical outcome, the mortality rate from acid ingestion of 14% has been reported as significantly higher than that associated with the ingestion of alkalis of 2%, as has the incidence of more severe injuries .…”

Section: Discussionmentioning

confidence: 99%

Caustic Ingestion—A Forensic Overview

Byard

2015

Journal of Forensic Sciences

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The ingestion of corrosive substances may produce severe burns to the upper aerodigestive tract and stomach, particularly if the pH is greater than 12 or less than two. There is a biphasic age grouping with adult cases most often involving self-harm and pediatric cases accidental ingestion. Three cases are reported to demonstrate characteristic features following the ingestion of potassium hydroxide, glacial acetic acid and Lysol(®) , respectively. All deaths were due to the effects of caustic burns to the upper aerodigestive tract, esophagus and stomach with perforation and/or hemorrhage. The extent of injuries in these cases depends on the nature, amount, and concentration of the agent and on the exposure time. A point to note at autopsy is that tissue damage may also occur from postmortem exposure. Typical injuries involve perioral, limb, and trunk burns, with extensive aerodigestive liquefactive/coagulative necrosis causing hemorrhage and perforation.

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Section: Discussionmentioning

confidence: 99%

Caustic Ingestion—A Forensic Overview

Byard

2015

Journal of Forensic Sciences

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“…Ingestion of pure methanol determines severe injuries to the upper digestive tract. Complete detachment of the oesophagus mucosa and brownish discolouration of the gastric mucosa with diffuse haemorrhagic necrosis of the stomach mucosa and intense acute inflammatory infiltration of the lamina propria have been described in a woman after suicidal ingestion of 500 ml absolute methanol that died 23 hours later due to metabolic acidosis and multiple organ dysfunction syndrome [4].…”

Section: Discussionmentioning

confidence: 99%

“…Coma and death may occur after substantial exposures. The minimum lethal dose following ingestion is considered to be in the range of 300-1000 mg/kg or a quantity of 50 -100 ml of pure methanol [2,3,4,5]. Several studies focusing on fatal methanol intoxication cases demonstrated an absolute prevalence of male gender, ranging between 80 -90% [6,7].…”

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confidence: 99%

A rare case of fatal materno-fetal methanol poisoning. Volatile congeners analysis as forensic evidence

Jung¹,

Idor²,

Bucur³

et al. 2014

RJLM

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Background. Methanol intoxication may be the result of either accidental or intentional ingestion, in case of substantial exposures coma and death may occur. Methanol poisoning during human pregnancy was rarely described. Material and method. We present the case of a 39-years old pregnant woman hospitalized for severe methanol intoxication. We reviewed the entire hospital medical documentation and performed blood and gastric content analysis for alcohol congeners using validated headspace-gaschromatography method (samples collected at admission from mother and at autopsy from fetus); we also examined all organs of the mother and of the stillborn, including microscopic sections stained with haematoxylin-eosin. Results and discussions. The 34 weeks pregnant patient was transported to the hospital due to respiratory distress, lethargy and coma. Laboratory findings revealed metabolic acidosis with anion gap. At presentation intrauterine fetal death was diagnosed and the fetus was extracted next day. The woman died after four days in hospital. At post-mortem examination we found marked brain edema, brain stem hemorrhages, focal bleedings in the white matter of the temporal and parietal lobes, leptomeningeal hyperaemia, kidneys with tubular necrosis and hemorrhages in renal cortex. Autopsy of the fetus revealed only leptomeningeal hyperaemia, suggesting a rapid death. Blood ethanol concentration was 1.03 g/l in mother and 1.98 g/l in foetus while methanol concentration was 1.72 g/l and 1.99 g/l respectively. Relatively high amounts of amyl-alcohol (2-methyl 1-butanol) in both samples indicate consumption of fruit distillate, while toxic blood methanol concentration can be explained only by contaminated beverage consumption. Conclusions. Intrauterine fetal death may occur without important morphological lesions in case of methanol transplacentar intoxication. Methanol is rapidly transferred to the fetus and cumulates in fetal circulation, while in case of other volatile congeners the transfer through the placental barrier seems to be selective.

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“…Methanol is a potent neurotoxin that can cause severe metabolic acidosis and serious neurological disorders. 18 Small quantities of pure methanol cause blindness and death, and the minimum lethal dose is 50-100 mL. 19 Methanol and its metabolites, formaldehyde and formic acid, are associated with metabolic acidosis, visual dysfunction, and neurological symptoms.…”

Section: Discussionmentioning

confidence: 99%

In vitro study on cytotoxicity and intracellular formaldehyde concentration changes after exposure to formaldehyde and its derivatives

Qin

et al. 2013

Hum Exp Toxicol

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HeLa cells were exposed to formaldehyde and its metabolic derivatives, methanol, formic acid, and acetaldehyde, to investigate that the toxicity of formaldehyde is not caused by the chemical group. After 1 h of treatment with formaldehyde, mitochondrial assays showed that low concentrations (e.g. 10 μmol/L) of formaldehyde promoted growth of the HeLa cells, while higher concentrations (e.g. ≥62.5 μmol/L) inhibited cell growth; while all four chemicals at a concentration of 125 μmol/L affected cell growth, formaldehyde affected the largest. Reactive oxygen species concentration increased with the concentration of the exposure chemical. The endogenous formaldehyde content increased the most in the formaldehyde group, but in other three groups, it did not increase as the exposure concentration increased. Expression of dehydrogenase (formaldehyde dehydrogenase (FDH)) in the formaldehyde (10.40) and methanol (10.60) groups increased significantly compared with the control (1), while it was similar to the control in formic acid (0.90) and acetaldehyde (1.10) groups. Our results suggest that formaldehyde could affect cell activity and even enter cells. Exposure to formaldehyde changes the endogenous formaldehyde concentration in cells within 24 h, and this induces expression of FDH for formaldehyde degradation to maintain the formaldehyde balance. The toxicity of formaldehyde is not caused by the carbon atoms in the aldehyde, hydroxyl, or carboxyl groups. Formaldehyde is hypothesized to be an important signaling molecule in the regulation of cell growth and maintenance of the endogenous formaldehyde level.

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Severe necrosis of oesophageal and gastric mucosa in fatal methanol poisoning

Cited by 12 publications

References 22 publications

Caustic Ingestion—A Forensic Overview

Caustic Ingestion—A Forensic Overview

A rare case of fatal materno-fetal methanol poisoning. Volatile congeners analysis as forensic evidence

In vitro study on cytotoxicity and intracellular formaldehyde concentration changes after exposure to formaldehyde and its derivatives

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